FB2024_03 , released June 25, 2024
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Citation
Schlossherr, J., Eggert, H., Paro, R., Cremer, S., Jack, R.S. (1994). Gene inactivation in Drosophila mediated by the Polycomb gene product or by position-effect variegation does not involve major changes in the accessibility of the chromatin fibre.  Mol. Gen. Genet. 243(4): 453--462.
FlyBase ID
FBrf0074380
Publication Type
Research paper
Abstract
In Drosophila position effect variegation and Polycomb-dependent regulation of homeotic gene expression are phenomena in which genes are inactivated in a clonally inherited manner. In both processes inactivation involves proteins that interact with the chromosome at or close to the position of inactivated genes. Two models have been proposed to explain this form of genetic silencing. In one, cooperative concatamerisation of a large multisubunit protein complex packages the chromatin fibre into a higher order structure, which is inaccessible for the transcription apparatus. In the second, the chromatin fibre is left unaltered but the region to be silenced is assigned to a compartment within the nucleus to which not all transcription factors have access. To distinguish between these types of model we have used the ligation-mediated PCR procedure to quantitate the accessibility of restriction sites in the chromatin fibre in both the active and inactivated forms. By making use of appropriate mutations and tissues we show that the inactivation of genes by Polycomb or by position effect variegation is not accompanied by a substantial change in the accessibility of the fibre. These results favour models in which the inactivation is achieved by sequestration of the silenced region in a particular nuclear compartment rather than by a chromatin packaging model.
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Gen. Genet.
    Title
    Molecular and General Genetics
    Publication Year
    1967-2001
    ISBN/ISSN
    0026-8925
    Data From Reference
    Aberrations (1)
    Alleles (3)
    Genes (6)